Questioning the Bacterial Overgrowth Hypothesis of IBS: An Epidemiologic and Evolutionary Perspective.

MedLine Citation:

PMID:
21397724
Owner:
NLM
Status:
Publisher

Abstract/OtherAbstract:

Although studies indicate that small intestinal bacterial overgrowth (SIBO) is prevalent in irritable bowel syndrome (IBS), it remains unclear whether SIBO causes IBS. This review presents an epidemiologic and evolutionary inquiry that questions the bacterial overgrowth hypothesis of IBS, as follows: (1) although the hypothesis may be biologically plausible, there is also a strong rationale for competing hypotheses; it is unlikely that SIBO is the predominant cause of IBS in all comers, because competing explanations are sensible and defensible. Moreover, data indicate that the test used to promulgate the SIBO hypothesis - the lactulose hydrogen breath test - may not have measured SIBO in the first place. (2) We do not have evidence of SIBO being absent before IBS symptoms, and present after IBS emerges. (3) There is not a dose-response relationship between small intestinal microbiota and IBS symptoms. (4) The relationship between SIBO and IBS is highly inconsistent among studies. (5) Many effective IBS therapies do not address SIBO at all, yet have a more favorable "number needed to treat" than antibiotics. (6) IBS does not behave like a traditional infectious disease, suggesting that microbes may not principally cause the syndrome. (7) Other factors may confound the relationship between SIBO and IBS, including proton pump inhibitors. (8) Whereas the brain-gut hypothesis is evolutionary sensible, the bacterial hypothesis is harder to defend from an evolutionary perspective. The article concludes that bacteria may contribute to some IBS symptoms, but that bacteria cannot be the only explanation, and a causal link between SIBO and IBS is not secure.

Department of Gastroenterology, VA Greater Los Angeles Healthcare System; Division of Digestive Diseases, David Geffen School of Medicine at UCLA; Department of Health Services, UCLA School of Public Health; CURE Digestive Diseases Research Center; Center for Neurobiology of Stress, David Geffen School of Medicine at UCLA; UCLA/VA Center for Outcomes Research and Education.